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Mycobacteria attenuate nociceptive responses by formyl peptide receptor triggered opioid peptide release from

Heike L Rittner1, Dagmar Hackel, Philipp Voigt

  • 1Klinik für Anaesthesiologie mit Schwerpunkt Operative Intensivmedizin, Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.

Plos Pathogens
|April 4, 2009
PubMed

Insights

Mycobacteria activate neutrophils via formyl peptide receptors (FPR), triggering opioid peptide release that reduces inflammatory pain. Targeting FPR may offer new pain relief strategies.

Area of Science:

  • Immunology
  • Neuroscience
  • Pharmacology

Background:

  • Inflammation involves a balance of pain-promoting and pain-relieving mediators.
  • Opioid peptides, released by neutrophils, activate peripheral opioid receptors to reduce pain.
  • Mycobacterium butyricum is used to induce inflammatory pain in animal models.

Purpose of the Study:

  • To investigate if mycobacteria-derived agonists activate neutrophils via formyl peptide receptors (FPR) or toll-like receptors (TLR).
  • To determine if this activation leads to opioid peptide release and subsequent inhibition of inflammatory pain.

Main Methods:

  • Inflammatory pain was induced in rats using Mycobacterium butyricum.
  • Neutrophil involvement was assessed via depletion and receptor antagonist studies.
  • Opioid peptide release from human and rat neutrophils was measured in vitro.
  • Intracellular calcium signaling and signaling pathway inhibitors were utilized.

Main Results:

  • Neutrophil depletion, opioid receptor antagonists, and anti-opioid antibodies increased inflammatory pain.
  • Mycobacterium butyricum and formyl peptides, but not TLR agonists, triggered opioid peptide release.
  • Opioid peptide release was dependent on intracellular calcium and phosphoinositol-3-kinase (PI3K) signaling.
  • FPR antagonists increased inflammatory pain, while TLRs were not implicated.

Conclusions:

  • Mycobacteria activate neutrophils through FPR, leading to opioid peptide secretion and pain reduction.
  • This mechanism highlights a novel endogenous analgesic pathway.
  • Selective FPR agonists represent a potential therapeutic target for managing inflammatory pain.

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